circRPS28 (hsa_circ_0049055) is a novel contributor for papillary thyroid carcinoma by regulating cell growth and motility via functioning as ceRNA for miR-345-5p to regulate frizzled family receptor 8 (FZD8).

Circular RNA 40S ribosomal protein S28 (circRPS28; hsa_circ_0049055) is upregulated in papillary thyroid carcinoma (PTC) patients. However, its role remained uncovered in the progression of PTC. Above all, expression of circRPS28 was determined in PTC samples by real-time quantitative PCR and circRPS28 was highly expressed in tumor tissues and cells. Besides, circRPS28 was predominantly distributed in the cytoplasm. Functional experiments were launched using colony formation assay, 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, 5-ethynyl-2-deoxyuridine (EdU) assay, transwell assays, scratch wound assay, and flow cytometry. As a result, blocking circRPS28 restrained PTC cell viability, EdU positive cell rate, colony formation number, wounding healing rate, and numbers of migration and invasion cells, accompanied with apoptosis rate promotion. These effects paralleled with low B-cell lymphoma (Bcl)-2 level and high Bcl-2-associated X protein (Bax), matrix metalloproteinase-2 (MMP2), and MMP9 levels, as analyzed by western blotting. Overexpressing microRNA (miR)-345-5p exerted similar roles to circRPS28 silencing. Notably, dual-luciferase reporter assay and RNA immunoprecipitation confirmed the target relationship between circRPS28 and miR-345-5p, miR-345-5p and frizzled family receptor 8 (FZD8). Downregulating miR-345-5p abrogated effects of circRPS28 blockage in PTC cells, and restoring FZD8 counteracted miR-345-5p roles, either. Furthermore, xenograft tumor model was established in mice, and exhausting circRPS28 delayed the growth of PTC cells in vivo by regulating miR-345-5p and FZD8. In conclusion, we demonstrated that blocking circRPS28 and/or promoting miR-345-5p suppressed PTC cell growth and motility via regulating FZD8. This study might suggest a novel circRPS28/miR-345-5p/FZD8 competing endogenous RNA pathway in PTC.